Ameliorating of Transcription Level of gp91Phox and P22Phox Subunits of NADPH Oxdisae Complex in Hypertrophied Heart of Rats by Resveratrol

Hypertension induced-left ventricular hypertrophy (LVH) is, at least initially, an adaptive response of the heart to pressure overload but it leads to heart failure if left untreated. Over-activity of reactive oxygen species generator, NADPH oxidase enzyme, is intricately linked with LVH progression.

The aim of the present study was to investigate the effect of, natural polyphenole, resveratrol on transcription level of NADPH oxidase subunits (gp91Phox, P22Phox, P67Phox, P47Phox and Rac1) in hypertrophied heart of rats.

Male Wistar rats were divided into the following groups: control (intact animal); sham (DMSO+H), untreated hypertrophy (H) and resveratrol-treated hypertrophy (R+H) groups. LVH was induced by abdominal aortic banding. Blood pressure was measured directly through carotid artery cannulation. Gene expression was evaluated using real time RT-PCR technique.

The animals in H group had higher systolic (SBP) and diastolic blood pressure (DBP) compared with control (P <0.001). In treated group (R+H) SBP and DBP were decreased significantly in comparison with H group (P <0.001). In H group, cardiac mRNA levels of gp91Phox, P22Phox, P67Phox and Rac1 subunits levels were upregulated by 98.4 ± 14.5%, 64.7 ± 8.8%, 36.4 ± 5% and 73.2 ± 10.8% ,respectively (P < 0.001, P < 0.001, P < 0.05 and P < 0.001, respectively vs. control). However in R+H group gp91Phox, P22Phox and Rac1 mRNA levels were 43.2 ± 4.5%, 28.6 ± 5.7% and 30.5 ± 5.8% which showed a significant difference compared with H group (P < 0.01, P < 0.05 and P < 0.05, respectively).

Transcription level of NADPH oxidase subunits increases in hypertrophied heart. Resveratrol protects the heart against pressure overload-induced LVH partly through downregulation of NADPH oxidase subunits.